2011/01/01 by Osamu Handa, Yuji Naito, Toshikazu Yoshikawa · 1 citation
Medicine · Veterinary · Immunology and Microbiology · #Helicobacter pylori-related gastroenterology studies #Veterinary medicine and infectious diseases #Galectins and Cancer Biology
paper · pdf · doi:10.1179/174329211x12968219310756
openalex publication_date 2011/01/01 · openalex created_date 2016/06/24 · openalex updated_date 2026/07/29
Almost half the world's population is infected by Helicobacter pylori (H. pylori). This bacterium increases the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in human stomach, and this has been reported to impact upon gastric inflammation and carcinogenesis. However, the precise mechanism by which H. pylori induces gastric carcinogenesis is presently unclear. Although the main source of ROS/RNS production is possibly the host neutrophil, H. pylori itself produces O₂•⁻. Furthermore, its cytotoxin induces ROS production by gastric epithelial cells, which might affect intracellular signal transduction, resulting in gastric carcinogenesis. Excessive ROS production in gastric epithelial cells can cause DNA damage and thus might be involved in gastric carcinogenesis. Understanding the molecular mechanism of H. pylori-induced carcinogenesis is important for developing new strategies against gastric cancer.